A major impediment in understanding prostatic cancer has been the lack of suitable experimental model. However, a unique animal model has been developed in our Institute and is characterized by tumors in a high incidence (up to 92%), with a relatively low latency (45 weeks) and with morphologic similarities to those occurring in man within 59 weeks. Moreover, prostatic cancer can be induced selectively in most animals by only limited doses of the carcinogen in combination with testosterone (T). Since epidemiologic data suggest an involvement of factors other than T (most probably high fat diet), we intend to examine this possibility by the following experiments. Seven groups of male Wistar-derived MRC rats (30 rats each) will be treated as follows: Group 1 (HF+T+BOP Group): Rats will be fed ad libitum a formulated high (corn oil) fat diet (HF; 18 g/385 Kcal) from 4 weeks of age for life. Rats will receive T for life beginning when they are 8 weeks of age. Two days after beginning T treatment, rats will receive daily BOP (20 mg/kg b.w. i.g.) for 3 days. Group 2 (CD+T+BOP Group): Rats will be treated as in Group 1, but they will be fed ad libitum a formulated control diet (CD) instead of the high fat diet. Group 3 (HF+BOP Group): In this group, rats will be fed and treated like Group 1 rats, except that no T will be given. Group 4 (CD+BOP Group): Rats will be treated like those in Group 1, except that they will be fed CD instead of the HF diet and no T will be given. Group 5 (HF+T Group): Rats will receive T in the same way as those in Group 1, but no BOP will be given. Group 6 (CD+T Group): Rats will be treated as those in Group 5, except that they will be fed CD instead of HF diet. Group 7 (CD Group) will serve as an untreated control group. Serum will be collected at 10 weekly intervals from all rats and stored frozen for later hormonal studies if effects of HF diet on prostatic carcinogenesis are seen. The results of these studies will give us the following information: 1) Does a HF diet potentiate the promoting effect of T on prostatic carcinogenesis by BOP (Group 1)? 2) Does a HF diet per se promote the prostatic carcinogenic effect of BOP (Group 3)? Does HF diet potentiate the prostatic carcinogenic effect of T? 4) Are changes in tumor incidence, caused by HF diet, correlated with changes in the serum hormone levels (i.e. T, estradiol (E), follicle stimulating hormone (FSH) and prolactin)?